Hypercalcemia in the Critically Ill Patient

Abstract

Hypercalcemia is now frequently recognized in hospitalized patients, including those who are critically ill. Hypercalcemia in critically ill patients may be life threatening or an indication of an underlying but unsuspected disease process. All of the common causes of hypercalcemia can occur in the critically ill patient and are reviewed here. As in the general patient population, the two most common causes are probably malignant disease and primary hyperparathyroidism. Hypercalcemia is now readily reversible in most patients, particularly when the underlying pathophysiologic mechanisms responsible are recognized, and it should be treated actively.In the initial evaluation of hypercalcemia in a critically ill patient, the physician must decide if the elevated serum calcium level is responsible for the patient's condition or is merely an incidental finding that poses no immediate danger. Patients in the former category are said to be in hypercalcemic crisis, and they require immediate treatment to lower their serum calcium levels, which are life threatening. In the intensive care setting, hypercalcemic crisis is most commonly associated with primary hyperparathyroidism or malignancy. With the advent of automated screening procedures, asymptomatic hypercalcemia is frequently seen in hospitalized patients as well as outpatients [1], and mild hypercalcemia is at least as common in intensive care patients as in other patient populations. In this article we review the pathogenesis and treatment of the various conditions associated with hypercalcemia, particularly those diseases that are more likely to be seen in a critically ill patient. PathogenesisNormally, plasma calcium levels are maintained within narrow limits by the parathyroid hormone (PTH) and 1,25-dihydroxyvitamin D. Hypocalcemia triggers PTH release, which (1) stimulates 1,25-dihydroxyvitamin D synthesis by the kidney and leads to increased intestinal calcium absorption, (2) directly stimulates osteoclastic bone resorption, and (3) increases calcium reabsorption in the distal tubules of the kidney. Hypercalcemia occurs when increased bone resorption or gut absorption of calcium leads to an influx of calcium into the extracellular fluid, which overwhelms the compensatory homeostatic mechanisms that maintain the serum calcium in the normal range. Hypercalcemia itself may cause vomiting and a decrease in the renal concentrating mechanism. This leads to dehydration and further increases in plasma calcium levels.